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Mario D Gonzalez

Publications and source records attributed to Mario D Gonzalez.

9 recordsLinked to original sources
PubMed2005

Rate-dependent block in the sinus venosa of the swine heart during transverse right atrial activation: correlation between electrophysiologic and anatomic findings.

UNLABELLED: Rate-dependent block in the sinus venosa. INTRODUCTION: Whether the crista terminalis or the sinus venosa result in rate-dependent block during transverse activation of the right atrial activation remains unknown. In the present study, right atrial activation at different cycle lengths was studied in the swine heart using high-resolution noncontact mapping (Endocardial Solutions). The location of the block was tagged and correlated with postmortem anatomical findings. METHODS AND RESULTS: Eight pigs were studied using noncontact mapping to obtain right atrial geometry and detailed sequence of activation using noncontact endocardial mapping. During sinus rhythm, activation proceeded uninterrupted craniocaudally along the sinus venosa and crista terminalis with similar conduction velocities (1.08+/-0.17 and 1.17+/-0.14 m/sec, respectively). Proximal coronary sinus stimulation was used to create transverse activation of the posterior right atrial wall. A rate-dependent decrease in conduction velocity occurred in the sinus venosa region (0.93+/-0.21, 0.82+/-0.14, and 0.52+/-0.09 m/sec at 500, 400, and 300 ms, respectively; P<0.05). The line of block verified by isopotential mapping and double potentials was obtained at cycle lengths of 240+/-30 ms. This line of the block was tagged with radiofrequency current lesions. Postmortem, all lesions were located in the sinus venosa region, 9.8+/-4.1 mm from the posteromedial edge of the crista terminalis. This region showed abrupt changes in muscle fiber thickness and orientation as well as in collagen content. CONCLUSIONS: The sinus venosa and not the crista terminalis results in a rate-dependent line of block during transverse right atrial activation. The morphologic characteristics of the sinus venosa appear to facilitate block in this region.

Animals↗
PubMed2004

Left atrial tachycardia originating from the mitral annulus-aorta junction.

BACKGROUND: At the mitral annulus-aorta (MA-Ao) junction, the left atrium is continuous through the subaortic curtain with the musculature of the anterior mitral leaflet. Under experimental conditions, this region can generate abnormal electrical activity. In patients with left atrial tachycardia, we investigated whether this region could be the source of this arrhythmia. METHODS AND RESULTS: In 10 (28%) of 35 consecutive patients with left atrial tachycardia, the arrhythmia originated from the MA-Ao junction. Sustained, self-limited episodes of atrial tachycardia (cycle length, 340+/-56 ms; duration, 125+/-69 seconds) were repeatedly induced. Prematurity of the extrastimulus and time to first atrial tachycardia complex were directly correlated (R=0.66; P<0.001). During tachycardia, bipolar electrograms at the earliest site preceded onset of the P wave by 44+/-14 ms and were of longer duration and lower amplitude than those recorded from nearby left atrial sites (52+/-8 versus 24+/-4 ms, P<0.001; and 0.53+/-0.08 versus 3.45+/-0.96 mV, respectively; P<0.001). Ablation eliminated the tachycardia with no recurrence after a mean follow-up of 24+/-19 months. A comparative study in mouse embryos demonstrated the presence of the developing specialized conduction system in the MA-Ao region starting at embryonic age 11.5. CONCLUSIONS: The MA-Ao junction can be a frequent source of left atrial tachycardia. This previously unrecognized site of origin may explain why catheter ablation has been less successful in eliminating left versus right atrial tachycardias. Remnants of the developing specialized conduction system could be the underlying substrate of this arrhythmia.

Adrenergic beta-Agonists↗
PubMed2003

Termination of paroxysmal supraventricular tachycardia by tecadenoson (CVT-510), a novel A1-adenosine receptor agonist.

OBJECTIVES: The aim of this study was to evaluate tecadenoson safety and efficacy during conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm. BACKGROUND: Tecadenoson (CVT-510), a novel adenosine receptor (Ado R) agonist, selectively activates the A1 Ado R and prolongs atrioventricular (AV) nodal conduction at doses lower than those required to cause A2 Ado R-mediated coronary and peripheral vasodilation. Unlike adenosine, which non-selectively activates all four Ado R subtypes and produces unwanted effects, tecadenoson appears to terminate AV node-dependent supraventricular tachycardias without hypotension and bronchoconstriction. METHODS: In this open-label, multicenter, dose escalation study, tecadenoson was administered to 37 patients (AV node re-entrant tachycardia, n = 29; AV re-entrant tachycardia, n = 8) with inducible PSVT sustained for > or =1 min during an electrophysiology study. Seven regimens (0.3 to 15 microg/kg) of up to two identical tecadenoson intravenous bolus doses were administered. RESULTS: After the first or second bolus, PSVT converted to sustained sinus rhythm for > or =5 min in 86.5% (32/37) of the patients, with 91% (29/32) of the conversions occurring after the first bolus (most within 30 s), coincident with anterograde conduction block in the AV node. No effects on sinus cycle length (SCL) or systolic blood pressure were observed. The atrial-His (AH), but not the His-ventricular (HV) interval was prolonged up to 5 min after the final tecadenoson bolus, returning to baseline by 10 min. Tecadenoson was generally well tolerated. CONCLUSIONS: In this study, tecadenoson rapidly terminated sustained PSVT by depressing AV nodal conduction without causing hypotension. After sinus rhythm restoration, there was minimal AH interval prolongation without HV interval or SCL prolongation.

Adenosine↗
PubMed2003

V-A block during atrioventricular nodal reentrant tachycardia: reentry confined to the AV node.

Retrograde block during atrioventricular (AV) nodal reentrant tachycardia is considered a rare phenomenon that can potentially occur in the AV node or in the atrium. A patient with slow-fast AV nodal reentrant tachycardia and transient VA block localized in the AV node is presented. Pharmacological and stimulation maneuvers identified the site of block in the AV node and not in the atrium. Thus, AV nodal reentry can be confined to the AV node.

Adult↗
PubMed2002

Demonstration of a left atrial input to the atrioventricular node in humans.

BACKGROUND: During right atrial stimulation, the anterior and posterior approaches provide inputs to the atrioventricular (AV) node. The purpose of the present study was to determine how activation proceeding from the left atrium reaches the AV node. METHODS AND RESULTS: We studied AV nodal conduction during right and left atrial (coronary sinus) stimulation in 46 patients (27 women and 19 men; mean age, 46+/-4 years) who had structurally normal hearts. At an identical cycle length (600 ms), left atrial stimulation resulted in shorter A-H intervals than right atrial stimulation (73+/-3 ms versus 99+/-3 ms; P<0.05). In addition, atrial electrograms recorded close to the His bundle changed from near to far field potentials when stimulation was shifted to the left atrium. The A-H interval prolonged as the site of pacing was progressively moved from the distal to the proximal coronary sinus. During constant pacing from the distal coronary sinus, atrial activation close to the His bundle could be advanced by late extrastimuli delivered at the anterior and posterior approaches (up to 11+/-2 ms and 9+/-1 ms, respectively), without altering His bundle activation time. In contrast, late extrastimuli delivered at the inferoparaseptal mitral annulus advanced both the A and H electrograms in 19 of 20 patients, which is consistent with a left-sided input to the AV node. Right and left atrial stimulation resulted in similar AV nodal function. CONCLUSION: The mitral annulus provides a left atrial input to the human AV node.

Atrial Flutter↗
PubMed2002

Right bundle-branch block unmasking a myocardial infarction.

A patient with an acute anteroseptal myocardial infarction and intermittent right bundle-branch block is presented. Abnormal Q waves in right precordial leads were only observed during right bundle-branch block. In the absence of right bundle-branch block, depolarization of the right ventricular free wall concealed the abnormal Q waves typical of an anteroseptal infarct. Right bundle-branch block, by preventing early activation of the right ventricular free wall, facilitated the correct diagnosis and localization of the infarction.

Aged↗
PubMed2002

Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: response of control patients to incremental doses of adenosine.

BACKGROUND: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electrophysiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. HYPOTHESIS: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. METHODS: Thirty-seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. RESULTS: The mean (+/- standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 +/- 3.9 and 7.4 +/- 4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0-8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. CONCLUSION: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.

Adenosine↗
PubMedDate not supplied

Rate control vs. pulmonary vein isolation.

Atrial fibrillation (AF) is a frequent arrhythmia encountered in clinical practice. It can be asymptomatic in some patients but incapacitating in others. Regardless of symptoms, patients at increased risk of embolism need chronic anticoagulation. In patients with AF and a rapid ventricular response that cannot be controlled with drugs, interventional procedures are required. Radiofrequency catheter ablation of the atrioventricular junction with pacemaker implantation is an effective therapeutic approach that relieves the symptoms associated with a rapid and irregular rhythm. This approach can also improve left ventricular function in patients with tachycardia-induced cardiomyopathy. Due to the irreversible nature of this approach, it is more suitable for older patients and those with advanced left ventricular dysfunction. Many patients with a structurally normal heart have symptomatic paroxysmal AF refractory to antiarrhythmic agents. This form of AF is frequently initiated by premature atrial beats arising from the pulmonary veins. A catheter ablation technique is available to electrically isolate the pulmonary veins. This procedure can eliminate AF in many patients but can result in complications, including embolic events, pulmonary veins stenosis, and cardiac perforation.

Atrial Fibrillation↗